Affiliations:
Departments of Pathology and Gastroenterology, Tokai University School of Medicine, Bohseidai, Isehara-shi, Kanagawa 259-1193, Japan

Published online on:Tuesday, June 1, 2004

Pages:773-777DOI:10.3892/ijmm.13.6.773

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Abstract

Gastritis and peptic ulcers result from Helicobacter pylori (H. pylori) infection. To analyze the influence of Helicobacter on inflammatory responses and cell proliferation, we used an animal model of H. pylori-induced gastritis in p53-knockout mice. H. pylori were introduced by gastric intubation into p53-knockout C57BL/6 mice. The animals were then followed-up for 1 year and compared with uninfected controls of the same genotype. Serum levels of anti-H. pylori antibody and histopathological changes were analyzed according to the updated Sydney System. Immunohistochemistry for proliferating cell nuclear antigen (PCNA) and TUNEL staining were also performed. The infected mice showed significantly increased levels of anti-H. pylori antibody in serum. Histologically, p53-knockout mice exhibited increased scores of chronic and active inflammation compared with uninfected controls. The PCNA and TUNEL indices were 25.5% and 10/mm, respectively, in the inflammatory foci of infected mice, and were increased compared with the controls. In the p53-knockout mice, H. pylori infection caused severe inflammatory reactions. The p53 gene may play an important role in inflammatory responses including cell proliferation and apoptosis.